The contour of the central arterial blood pressure pulse of an adult is different from the contour of the pressure pulse of a youth. The pressure pulse of an adult has an augmented peak in late systole, and a near-exponential decay during diastole, while the pressure pulse of a youth has a rounded peak throughout systole and a second peak during diastole.
The differences in the two pressure pulse patterns are attributable largely to an early return in an adult of a secondary reflection wave, that is, a reflection of the primary pressure pulse along the arterial tree from the periphery in the lower part of the body. The early return of the secondary wave is due to an increase in the velocity of the arterial pulse caused by a stiffening and/or mismatch of the conduit arteries in the adult. Because of its early return, the secondary wave arrives at the heart during its contraction, and thus augments the systolic peak of the pressure pulse in the left ventricle of the heart, in the ascending aorta and in other proximal arteries.
A youth has arteries which are more distensible, and therefore, the arterial pulse wave is slower in the youth than in the adult. Thus the secondary wave from the lower body does not return as early in the pulse cycle, and therefore, it does not combine with, or augment, the systolic peak of the central pressure pulse. Instead, the pulse has a second peak in diastole which corresponds to the later return of the secondary wave.
With increasing age, characteristic changes can be seen in the contour and amplitude of the pressure pulse in both the central and the peripheral arteries, due largely to the earlier return of the secondary (reflected) wave from the lower body. From the fourth decade on, a relatively large augmentation of the pulses in late systole can be observed in the carotid and ascending aorta, and left ventricle. Such augmentation is not observed, or not observed to the same degree, in the pulses in the peripheral arteries of the upper limb, however, until the eighth decade. Thus, measurements of blood pressure in the peripheral arteries of the upper limb are not completely accurate representations of the pressure in the carotid artery or ascending aorta.
The discrepancies in pressure between central and peripheral arteries help to explain why, in arterial hypertension, the degree of arterial damage and the severity of left ventricular hypertrophy do not always correlate well with the level of brachial systolic pressure. The discrepancies also explain why regression of left ventricular hypertrophy induced by various drugs does not always accord with the degree of reduction in brachial arterial pressure.
The usual clinically-accepted method for determination of the hydraulic load presented to the left ventricle in man is through measurement of systolic arterial pressure in the brachial artery with a sphygmomanometer. The clinician then uses the measured systolic pressure as an indication of the maximum pressure in all major arteries of the body and in the left ventricle of the heart. Such an assumption is not justified, however, because of the differences in the effect of wave reflection in the periphery of the body and the central arteries, as discussed above.
While these problems with blood pressure interpretation are generally known, no one has previously developed a noninvasive measurement method which is more accurate than the sphygmomanometer for assessment of central aortic pressure, or of left ventricular pressure during systole. Yet it is highly desirable to be able to ascertain augmentation of pressure pulses in the ascending aorta from an analysis of the contour of the primary and secondary pressure waves in peripheral arteries. This would allow physicians to diagnose and treat more appropriately abnormal blood pressure and arterial conditions early in life, and thus, aid the physicians in preempting the dangerous effects of such conditions in later life. It would also assist in treating established disease including cardiac failure, angina pectoris and hypertension, and for investigating left ventricular function.